These situations could include mutations in noncoding regions of the ALPL gene; defects in transcription factors such as RUNX2, which is involved in the regulation of TNSALP and therefore in the regulation of bone mineralization, presenting phenotypes that may overlap with those of HPP; or other secondary causes unconsidered to date such as hemochromatosis. The gene discussed is RUNX2; the disease is hemochromatosis.